Display Settings:

Format

Send to:

Choose Destination
J Biomech. 1996 Jan;29(1):69-79.

Cyclic mechanical property degradation during fatigue loading of cortical bone.

Author information

  • 1Department of Orthopaedics, Case Western Reserve University, Cleveland, OH 44106, USA.

Abstract

Fatigue damage accumulation has been demonstrated in living bone and postulated as a stimulus to the bone modeling and remodeling response. Mechanical property degradation is one manifestation of fatigue damage accumulation. This study examines changes in secant modulus and cyclic energy dissipation behavior during axial load-controlled fatigue loading of cortical bone specimens. The findings suggest that secant modulus degradation and cyclic energy dissipation are greatly increased at loading levels above critical damage strain thresholds of 2500 and 4000 mu epsilon in tensile and compressive fatigue, respectively. Tensile and compressive fatigue loading also caused different forms of modulus degradation at loading levels above these thresholds. Bone behaves as a linear viscoelastic material below these thresholds, even after prior property degradation at higher loading levels. Cyclic energy dissipation was proportional to the 2.1 power of the applied effective strain range for all loadings below 2500 mu epsilon. Above 2500 mu epsilon, tensile fatigue loading caused cyclic energy dissipation proportional to the 5.8 power of the applied effective strain range. Compressive fatigue loading dissipated cyclic energy proportional to the 4.9 power of applied effective strain range over 4000 mu epsilon. Lifetime energy dissipation over all fatigue tests to fracture at a single loading level was well fitted by the same power law in the number of cycles to failure raised to the 0.6 power. Loading levels of 2500 mu epsilon in tension and 4000 mu epsilon in compression are within the ranges observed in living animals, and thus these phenomena may play a role in initiating the remodeling response in live bone tissue.

PMID:
8839019
[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Icon for Elsevier Science
    Loading ...
    Write to the Help Desk